First Hospital of Lanzhou University

To address the current lack of standardized protocols for vestibular infant screening (VIS), this clinical consensus aims to establish a clinical consensus on VIS in infants aged 0-12 months. Given a frequent co-occurrence of vestibular dysfunction in children with sensorineural hearing loss (SNHL) and the significant impact of vestibular dysfunction on early development, early identification and management are critical. This clinical consensus was developed by a panel of 28 international experts in pediatric otolaryngology and vestibular disorders through a structured, multi-round Delphi process. Panelists were selected based on clinical and academic expertise, representing 26 institutions across Asia and Europe. A comprehensive literature review (2000-2024) informed the initial draft of consensus statements. The consensus was reached through three iterative rounds of anonymous rating and feedback, followed by virtual discussions. Statements achieving ≥ 80% agreement were retained in the final consensus, which focused on screening tools, target populations, optimal timing, and standardized cVEMP recording protocols for infants. The expert panel reached consensus on key recommendations in four domains: screening tool, target screening population, timing of vestibular function screening, and recording protocol for cervical vestibular evoked myogenic potential (cVEMP). This clinical consensus provides foundational guidance for the implementation of VIS in infants, advocating for standardized protocols to improve early diagnosis and intervention. Widespread adoption of these recommendations may enhance developmental outcomes by enabling timely detection and management of vestibular dysfunction in early childhood.

Objective To analyze the relationships among the surface antigens of lymphocytes in patients with sepsis, the level of thrombospondin-1 (THBS1), and myocardial injury. Methods 360 sepsis patients who were hospitalized to our hospital between January 2023 and January 2025 were chosen. 170 patients with myocardial injury and 190 patients without myocardial injury were selected from the patient group based on whether or not they had myocardial injury. Serum THBS1 levels, immune function (CD4+, CD8+, and CD4+/CD8+), myocardial injury markers (creatine kinase MB (CK-MB), heart-type fatty acid binding protein (H-FABP), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and cardiac troponin I (cTnI)), and echocardiographic markers (left ventricular ejection fraction (LVEF), early diastolic velocity to atrial contraction velocity ratio (E/A), and cardiac output (CO)) were compared. Correlations between immune function, THBS1 levels, myocardial injury indicators, and echocardiographic markers in individuals with myocardial damage and infection were examined. To predict sepsis with myocardial infarction, the serum THBS1 value was evaluated using the receiver operating characteristic (ROC) curve and the area under the curve (AUC). Results While the myocardial injury group had significantly lower levels of CD8+ T cells in peripheral blood, LVEF, E/A, and CO, the nonmyocardial injury group had significantly higher levels of CD4+, CD4+/CD8+, serum THBS1, CK-MB, H-FABP, NT-proBNP, and cTnI (P<0.05). Patients with sepsis and myocardial injury had considerably higher peripheral blood CD8+ T cell counts with LVEF, E/A, and CO (P<0.05) and significantly lower counts with CK-MB, H-FABP, NT-proBNP, and cTnI (P<0.05). CK-MB, H-FABP, NT-proBNP, and cTnI were strongly positively correlated (P<0.05) with peripheral blood CD4+ and CD4+/CD8+ T cell counts, while LVEF, E/A, and CO were significantly correlated negatively (P<0.05). Serum THBS1 levels had a substantial negative correlation (P<0.05) with LVEF, E/A, and CO and a strong positive correlation (P<0.05) with CK-MB, H-FABP, NT-proBNP, and cTnI. With a sensitivity of 80.03% and specificity of 87.43%, the serum THBS1 concentration demonstrated an AUC of 0.892 (95% CI: 0.857–0.947) for predicting both sepsis and myocardial damage. Conclusion Sepsis patients' levels of THBS1 and lymphocyte surface antigens are somewhat linked to myocardial damage, and THBS1 is anticipated to function as a biomarker for anticipating myocardial damage in sepsis patients.

Boron neutron capture therapy (BNCT) is an emerging binary targeted radiotherapy modality. This study evaluates the therapeutic potential of boronophenylalanine (BPA)-mediated BNCT in cervical cancer and to elucidate its underlying molecular mechanisms. A comprehensive set of in vitro and invivo approaches was employed using cervical cancer cell lines (HeLa, SiHa) and normal cervical epithelial cells (H8). The experimental techniques included clonogenic assays, flow cytometry, Western blotting, immunohistochemistry, and xenograft mouse models to assess cytotoxicity, boron uptake, DNA damage response, apoptosis, and therapeutic efficacy. Cervical cancer cells exhibited significantly higher L-type amino acid transporter 1 (LAT1) expression compared with normal controls, which correlated with enhanced BPA uptake. BPA-BNCT induced profound, dose-dependent cell death and reversed the conventional radiotherapeutic sensitivity profiles between cancer and normal cells. Notably, BNCT demonstrated selective cytotoxicity across different pathological subtypes of cervical cancer, with enhanced therapeutic efficacy observed in adenocarcinoma-a subtype typically resistant to conventional radiotherapy. Mechanistically, BNCT triggered complex DNA double-strand breaks that overwhelmed cellular repair mechanisms, despite robust activation of both homologous recombination (via RAD51) and nonhomologous end joining (via KU70/80). This irreparable DNA damage resulted in G2/M phase arrest and activation of the mitochondrial apoptosis pathway. In xenograft models, BPA-BNCT achieved significant tumor growth suppression and substantially prolonged survival, while maintaining a wide therapeutic window and showing no evidence of systemic toxicity. BPA-BNCT exerts potent and selective antitumor effects against cervical cancer through a dual mechanism: LAT1-mediated boron delivery ensures tumor specificity, while the resulting high-linear energy transfer radiation induces DNA damage that capitalizes on the inherent limitations of the tumor cells' DNA repair capacity, leading to catastrophic cell death. The therapy demonstrates a distinct advantage in treating adenocarcinoma subtypes, which are typically less responsive to conventional radiotherapy. These findings provide robust preclinical evidence supporting BNCT as a promising therapeutic approach, particularly for radiotherapy-resistant cervical adenocarcinoma.